Protective effects of 6,7,4′-trihydroxyisoflavone, a major metabolite of daidzein, on 6-hydroxydopamine-induced neuronal cell death in SH-SY5Y human neuroblastoma cells
- Authors
- Ko Y.-H.[Ko Y.-H.]; Kwon S.-H.[Kwon S.-H.]; Kim S.-K.[Kim S.-K.]; Lee B.-R.[Lee B.-R.]; Hur K.-H.[Hur K.-H.]; Kim Y.-J.[Kim Y.-J.]; Kim S.-E.[Kim S.-E.]; Lee S.-Y.[Lee S.-Y.]; Jang C.-G.[Jang C.-G.]
- Issue Date
- Dec-2019
- Publisher
- Pharmaceutical Society of Korea
- Keywords
- 6,7,4′-Trihydroxyisoflavone; 6-Hydroxydopamine; Apoptosis; Oxidative stress; Parkinson’s disease
- Citation
- Archives of Pharmacal Research, v.42, no.12, pp.1081 - 1091
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Archives of Pharmacal Research
- Volume
- 42
- Number
- 12
- Start Page
- 1081
- End Page
- 1091
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/13640
- DOI
- 10.1007/s12272-019-01191-4
- ISSN
- 0253-6269
- Abstract
- Daidzein, one of the important isoflavones, is extensively metabolized in the human body following consumption. In particular, 6,7,4′-trihydroxyisoflavone (THIF), a major metabolite of daidzein, has been the focus of recent investigations due to its various health benefits, such as anti-cancer and anti-obesity effects. However, the protective effects of 6,7,4′-THIF have not yet been studied in models of Parkinson’s disease (PD). Therefore, the present study aimed to investigate the protective activity of 6,7,4′-THIF on 6-hydroxydopamine (OHDA)-induced neurotoxicity in SH-SY5Y human neuroblastoma cells. Pretreatment of SH-SY5Y cells with 6,7,4′-THIF significantly inhibited 6-OHDA-induced neuronal cell death, lactate dehydrogenase release, and reactive oxygen species production. In addition, 6,7,4′-THIF significantly attenuated reductions in 6-OHDA-induced superoxide dismutase activity and glutathione content. Moreover, 6,7,4′-THIF attenuated alterations in Bax and Bcl-2 expression and caspase-3 activity in 6-OHDA-induced SH-SY5Y cells. Furthermore, 6,7,4′-THIF significantly reduced 6-OHDA-induced phosphorylation of c-Jun N-terminal kinase, p38 mitogen-activated protein kinase, and extracellular signal-regulated kinase 1/2. Additionally, 6,7,4′-THIF effectively prevented 6-OHDA-induced loss of tyrosine hydroxylase. Taken together, these results suggest that 6,7,4′-THIF, a major metabolite of daidzein, may be an attractive option for treating and/or preventing neurodegenerative disorders such as PD. © 2019, The Pharmaceutical Society of Korea.
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